Project description:Cryptocaryonosis caused by Cryptocaryon irritans is one of the major diseases of large yellow croaker (Larimichthys crocea), which lead to massive economic losses annually. The pathogenesis for cryptocaryonosis has been researched by a series of transcriptome studies under different infection conditions. However, little is known about the roles of tissue-specifically expressed genes during the infection of C. irritans. In this study, we analyzed the tissue-specific expression of transcripts in the major infection organs including gill and skin of L. crocea after C. irritans infection. we constructed transcriptome expression profiles of L. crocea gill and skin, including 23,172 protein-coding genes and 7,503 long noncoding RNAs (lncRNAs). By comparing transcriptome data from different tissues of L. crocea, we observed tissue specificity of transcripts in gill and skin, including 3,003 protein coding genes and 639 lncRNAs. A total of 212 of the protein coding genes were involved in immune system. Further analysis revealed that the tissue-specific DEGs in gill and skin were mainly involved in HIF-1 signaling pathway and Complement and coagulation cascades, respectively. In addition, 9 non-tissue-specific hub genes, including CCL4, DDIT4, LEP, ect., which are highly associated with C. irritans infection were identified. To our knowledge, this is the first comparative transcriptome analysis of gill and skin after C. irritans infection. Our results are helpful to understand the molecular mechanism of pathogenesis for cryptocaryonosis, espec-tissue specificity of protein-coding genes and lncRNAs involved in immune regulation.
Project description:Cryptocaryon irritans is the causative agent of white spot disease that infects virtually all marine teleost including Lates calcarifer. We undertook to gain an informative snapshot of the host’s transcriptomic response during the course of infection. Liver and spleen cDNA libraries-based L. calcarifer cDNA microarray were used as a tool to oversee the infection response. Parasites infection was carried out on juvenile fish for four days, and total RNA was extracted from the daily harvested infected liver. cDNAs synthesized from respective daily pooled total RNA were labelled and hybridized onto the L. calcarifer chip. The majority of infection-induced genes are acute phase proteins (APP) with hepcidin, C-type lectin and serum amyloid A being the most up-regulated products.
Project description:Cryptocaryon irritans causes marine "white spot disease" in various fish hosts, including the golden pompano, a highly sensitive species with significant economic value in the coastal regions of South China. Therefore, exploring the molecular mechanisms that C. irritans infection is important for accelerating molecular breeding programs. In this study, we artificially infected golden pompano with C. irritans. Morphological observations of the gills using tissue sections revealed significant histological changes following infection. RNA-seq was employed to profile gene expression in the gills of golden pompano at different time points post-infection to investigate the molecular mechanisms of the disease. After filtering low-quality sequences, a total of 781,496,198 clean reads were obtained, with Q30 greater than 95%. Differentially expressed genes (DEGs) were identified at 24 hours, 3 days, and 5 days post-infection, with 800, 4208, and 2712 DEGs, respectively. After combining and removing false positives, a total of 2968 DEGs were analyzed for spatiotemporal expression patterns, and these DEGs could be categorized into two down-regulated expression patterns. KEGG enrichment analysis revealed that DEGs were associated with cell-cell junctions, cell-ECM interactions, signal transduction, and immune-related pathways. Further analysis suggested that gill tissue damage during infection led to reduced dissolved oxygen intake, increasing physiological and metabolic stress. This was accompanied by widespread downregulation of collagen genes and deprivation of growth factors, indicating impaired tissue repair. Additionally, as an apoptosis inhibitor, Bcl-2 was found to be downregulated in the infected fish. Therefore, C. irritans infection-induced gill damage leads to hypoxia and subsequently triggers cellular apoptosis.
Project description:Numerous studies have demonstrated that the C. irritans can be efficiently propagated in the animal model golden pompano (Trachinotus blochii), especially in the process of intensive high-density culture, which causes large-scale infection and triggers bacterial invasion is a devastating blow to the golden pompano industry. This is in sharp contrast to the low sensitivity of S. oramin to C. irritans.
2022-10-23 | GSE186569 | GEO
Project description:Transcriptome of Cryptocaryon irritans tomonts